Interleukin-18 binding protein attenuates lipopolysaccharide-induced acute lung injury in mice via suppression NF-κB and activation Nrf2 pathway.

摘要: Abstract Interleukin (IL)-18 belongs to a rather large IL-1 gene family and is proinflammatory cytokine. IL-18 plays important roles in lung injury. binding protein (IL-18BP), natural antagonist of IL-18, binds with high affinity. IL-18BP able neutralize biological activity has protective effect against renal fibrosis. The aim this study was evaluate the potential on lipopolysaccharide (LPS)-induced acute injury (ALI) mice illuminate underlying mechanisms. Results indicated that pretreatment significantly attenuated LPS-induced pulmonary pathological Meanwhile, markedly inhibited infiltration inflammatory cell release factor ALI in vivo primary macrophages after LPS insult in vitro. treatment dramatically reduced oxidative stress through increasing superoxide dismutase (SOD) glutathione (GSH) contents, decreasing levels malondialdehyde (MDA) reactive oxygen species (ROS) macrophages. Additionally, also observed decreased activation nuclear factor-kappa B (NF-κB) upregulated erythroid 2-related 2 (Nrf2). Taken together, possessed ALI, which might be associated its regulation NF-κB Nrf2 activities. results rendered worthy further development into pharmaceutical drug for ALI.